Evidence map›Paper›PMID 20086015›Full record

ArticleThe Journal of biological chemistry2010

Podocyte injury induces nuclear translocation of WTIP via microtubule-dependent transport.

Jane H Kim, Martha Konieczkowski, Amitava Mukherjee, Sam Schechtman, Shenaz Khan, Jeffrey R Schelling, Michael D Ross, Leslie A Bruggeman, John R Sedor

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.1field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  8. Review
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  10. Review
  11. Article
  12. Review
  13. Current concepts of the podocyte in nephrotic syndrome.Kidney research and clinical practice · 2012
    Review
  14. Article
  15. Article
  16. APOL1 localization in normal kidney and nondiabetic kidney disease.Journal of the American Society of Nephrology : JASN · 2011
    Article
  17. Review
  18. Article
  19. Out on a LIM: chronic kidney disease, podocyte phenotype and the Wilm's tumor interacting protein (WTIP).Transactions of the American Clinical and Climatological Association · 2011
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Jane H KimDepartment of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44109.
Martha KonieczkowskiCase Western Reserve University Center for the Study of Kidney Disease and Biology, Cleveland, Ohio 44109.
Amitava MukherjeeCase Western Reserve University Center for the Study of Kidney Disease and Biology, Cleveland, Ohio 44109.
Sam SchechtmanCase Western Reserve University Center for the Study of Kidney Disease and Biology, Cleveland, Ohio 44109.
Shenaz KhanCase Western Reserve University Center for the Study of Kidney Disease and Biology, Cleveland, Ohio 44109.
Jeffrey R SchellingCase Western Reserve University Center for the Study of Kidney Disease and Biology, Cleveland, Ohio 44109; Department of Medicine, MetroHealth System Campus, Cleveland, Ohio 44109.
Michael D RossDepartment of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115.
Leslie A BruggemanCase Western Reserve University Center for the Study of Kidney Disease and Biology, Cleveland, Ohio 44109; Department of Medicine, MetroHealth System Campus, Cleveland, Ohio 44109.
John R SedorDepartment of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44109; Case Western Reserve University Center for the Study of Kidney Disease and Biology, Cleveland, Ohio 44109; Department of Medicine, MetroHealth System Campus, Cleveland, Ohio 44109. Electronic address: john.sedor@case.edu.
Case Western Reserve University · USBrigham and Women's Hospital · US

Funding

Mechanisms of tubular atrophy in renal diseaseR01DK067528 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI SCHELLING, JEFFREY R · 2005 to 2025
$7.1M
CWRU NEPHROLOGY TRAINING PROGRAMT32DK007470 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI SEDOR, JOHN R. · 1986 to 2019
$2.9M
TARGETING RENAL OUTER MEDULLARY K+ CHANNEL ROMK FOR NEW CLASS OF DIURETICSP50DK054178 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI SEDOR, JOHN R. · 1998 to 2002
$2.2M
Mechanisms of glomerular disesase progressionR01DK072348 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI SCHELLING, JEFFREY R · 2008 to 2012
$1.6M
Renal Disease Progression in African AmericansR01DK059997 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI SCHELLING, JEFFREY R · 2002 to 2005
$1.5M
Mechanisms of Glomerular ScarringR01DK064719 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI SEDOR, JOHN R. · 2003 to 2006
$1.2M
The WT1 Interacting Protein: a choreographer of morphology and transcriptionF30DK083897 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI KIM, JANE · 2009 to 2012
$141k
NIDDK NIH HHS DK-064719NIDDK NIH HHS DK-07470NIDDK NIH HHS F30 DK083897NIDDK NIH HHS P50 DK-054178NIDDK NIH HHS R01 DK059997NIDDK NIH HHS R01 DK064719NIDDK NIH HHS R01 DK067528NIDDK NIH HHS R01 DK072348NIDDK NIH HHS T32 DK007470
6 · The paper itself

Abstract

Podocyte structural and transcriptional phenotype plasticity characterizes glomerular injury. Transcriptional activity of WT1 (Wilm's tumor 1) is required for normal podocyte structure and is repressed by the podocyte adherens junction protein, WTIP (WT1 interacting protein). Here we show that WTIP translocated into podocyte nuclei in lipopolysaccharide (LPS)-treated mice, a model of transient nephrotic syndrome. Cultured podocytes, which stably expressed an epitope-tagged WTIP, were treated with LPS. Imaging and cellular fractionation studies demonstrated that WTIP translocated from podocyte cell contacts into nuclei within 6 h and relocalized to cell contacts within 24 h after LPS treatment. LPS-stimulated WTIP nuclear translocation required JNK activity, which assembled a multiprotein complex of the scaffolding protein JNK-interacting protein 3 and the molecular motor dynein. Intact microtubule networks and dynein activity were necessary for LPS-stimulated WTIP translocation. Podocytes expressing sh-Wtip change morphology and demonstrate altered actin assembly in cell spreading assays. Stress signaling pathways initiate WTIP nuclear translocation, and the concomitant loss of WTIP from cell contacts changes podocyte morphology and dynamic actin assembly, suggesting a mechanism that transmits changes in podocyte morphology to the nucleus.

Indexed as

Active Transport, Cell NucleusActinsAnimalsBiological TransportCarrier ProteinsCell LineCell NucleusCo-Repressor ProteinsCytoskeletal ProteinsHumansLipopolysaccharidesMiceMicrotubulesPhenotypePodocytesSignal TransductionActinsCarrier ProteinsCo-Repressor ProteinsCytoskeletal ProteinsLipopolysaccharidesWTIP protein, humanWtip protein, mouse

Identifiers

PMID20086015
PMCPMC2843245
OpenAlexW1970738130

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.